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Altered expression of bcl‐2 and bax mRNA in amyotrophic lateral sclerosis spinal cord motor neurons
Author(s) -
Mu Xiaojun,
He Jin,
Anderson David W.,
Springer Joe E.,
Trojanowski John Q.
Publication year - 1996
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410400307
Subject(s) - spinal cord , amyotrophic lateral sclerosis , lumbar spinal cord , motor neuron , neuroscience , in situ hybridization , biology , lumbar , medicine , anatomy , pathology , messenger rna , gene , biochemistry , disease
One of the primary neurodegenerative events occurring in amyotrophic lateral sclerosis (ALS) is the selective loss of spinal cord α motor neurons. To study the potential role of apoptosis in the degeneration of these motor neurons, in situ hybridization was used to measure the expression of two apoptotic cell death genes, bcl‐2 and bax , in control and ALS lumbar spinal cord sections. The strongest hybridization signal for bcl‐2 mRNA in neurological and nonneurological control spinal cords was found primarily in lamina IX α motor neurons, while a weaker hybridization signal was found in neurons of Clarke's nucleus and the proper sensory nucleus of the dorsal horn. Surviving lamina IX motor neurons in ALS spinal cord sections also expressed bcl‐2 mRNA, but at levels that were significantly and selectively decreased (4.7‐fold) compared with control. bax mRNA hybridization signal was detected in several cells throughout the gray matter in control and ALS lumbar spinal cord, but was significantly and selectively increased (2.8‐fold) in ALS motor neurons. Given the proposed interactive roles of these genes in apoptosis, the present findings favor a scenario in which this mode of cell death would contribute to spinal cord motor neuron degeneration in ALS.